Thursday, June 26, 2014

A 29 year old male with pleuritic chest pain for 6 hours

This case was sent to me by Taylor Sanders of the LSU- Baton Rouge Emergency Medicine residency.

A 29 year old complained of 6 hours of pleuritic chest pain:

QRS: There is rSR' in V1, consistent with RV conduction delay, but the QRS does not appear prolonged and there are no S-waves in lateral leads.  However, this absence of lateral S-wave may be due to terminal QRS distortion from the ST Elevation.

R-waves in Lateral leads: the R-waves in I and aVL are minimal, but are well formed in V5 and V6; this is somewhat unusual, and one must entertain the possibility of reversed limb lead placement.  However, when the axis is 90 degrees, because V5 and V6 are inferior to limb leads I and aVL, they may show R-waves when I and aVL do not.   

PR segments: there appears to be some PR depression in leads II and V3.  In lead II, it is partly due to a downsloping baseline.  This PR depression is suggestive of myo-pericarditis, but may also be found in MI.  PR depression of greater than 0.8 mm is generally considered specific for pericarditis, but the data upon which this is established comes from the pre-angiogram era, and cannot be fully trusted.

ST segments: 

There is marked ST elevation in inferior and lateral leads.  Inferolateral STEMI and pericarditis are very difficult to distinguish, and the best means to do so is that with inferolateral STEMI there is virtually always ST depression in aVL, even when there is ST elevation in V5 and V6.  There is no reciprocal ST depression in aVL and this makes inferior STEMI, even with superimposed lateral STEMI, very unlikely. 

The ST axis in pericarditis is rarely to the right of lead II.  An ST axis towards lead II results in no limb lead ST depression except in aVR (which is the opposite of a lead midway between I and II)

The ST axis in inferior STEMI is almost always to the right of lead II (resulting in ST depression in aVL) 

ST depression in aVR is found in all etiologies of inferior ST elevation: pericarditis, early repol and MI.  So this is not helpful.  However, there is ST depression in V1 and V2: is this posterior injury?  Or are these ST segments simply discordant to the R' wave, and a result of the abnormal depolarization ("secondary", not "primary" ST segment abnormalities)?  In general, myo-pericarditis does not have reciprocal ST depression anywhere except lead aVR, but this may be an exception due to the R' waves in V1 and V2.

T-waves: These are prominent, and worrisome for MI or early repolarization.  Early repolarization is possible, but less likely when not also seen in anterior leads.  Slow upstroke and fast downstroke, and relatively short QT favor a non-MI diagnosis as well.  T-waves in II, III, aVF and V4-V6 are very tall relative to the R-wave and QRS.

QTc interval: I do not have the computerized QTc for this case, but my visual inspection puts it at no longer than 380 ms.  In our as yet unplublished study of inferior STEMI, only 7% had a QTc less than or equal to 380ms. 

I was shown this ECG with just the clinical information above.  I responded that this is probably myo- or peri-carditis but that I was worried about the size of the T-waves.   And I often say the "you diagnose pericarditis at your peril."  The fact that the pain was pleuritic and the patient was 29 years old is supportive of pericarditis, but look at this case of a 24 year old woman with chest pain after a night of drinking and vomiting.

The first troponin I returned at 6 ng/mL (significantly elevated).

Another ECG was recorded:
Now there is much more ST elevation in lateral precordial leads.  There is also STE in aVL.  (ST axis is to the left of lead II; this is highly suggestive of pericarditis.  But how much do you want to bet?)
These are dynamic ST segments.  Are ST segments in pericarditis this dynamic?  I don't think we have a lot of data on this.  But this is very worrisome for STEMI, so the patient was taken emergently to the cath lab.

A very reasonable course of action would be a formal echocardiogram to look for wall motion abnormalities.  Absence of WMA would make STEMI impossible and establish the diagnosis of pericarditis without subjecting the patient to an angiogram.

It is also very reasonable to avoid any delay and go directly to the cath lab.

All coronary arteries were clean.

Final diagnosis:  Myocarditis

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